Chris J.L.M. Meijer

TL;DR: Data suggest that EBV in H‐RS cells is able to down‐regulate the expression of T‐ ( CD3) and B‐ (CD20) cell lineage markers and lymphoid activation markers (EMA and the 115D8 antigen) as compared with EBV‐negative cases.

TL;DR: A proposal is given for the diagnostic approach for infants with RRRMs detected in the antenatal period by means of ultrasonography, enabling an informed prognosis and subsequent genetic counselling.

TL;DR: It is suggested that EBV may be associated with the development of some cases of Hodgkin's disease and CD30-positive NHL and a correlation between the expression of LMP and the detection of CD30 in tumor cells of HD and NHL.

TL;DR: The findings suggest that AdCB016-mp53(268N) is a promising new agent for treatment of HPV-associated human cancers.

Abstract: Polycomb-group (PcG) genes preserve cell identity by gene silencing, and contribute to regulation of lymphopoiesis and malignant transformation. We show that primary nodal large B-cell lymphomas (LBCLs), and secondary cutaneous deposits from such lymphomas, abnormally express the BMI-1, RING1, and HPH1 PcG genes in cycling neoplastic cells. By contrast, tumor cells in primary cutaneous LBCLs lacked BMI-1 expression, whereas RING1 was variably detected. Lack of BMI-1 expression was characteristic for primary cutaneous LBCLs, because other primary extranodal LBCLs originating from brain, testes, and stomach were BMI-1-positive. Expression of HPH1 was rarely detected in primary cutaneous LBCLs of the head or trunk and abundant in primary cutaneous LBCLs of the legs, which fits well with its earlier recognition as a distinct clinical pathological entity with different clinical behavior. We conclude that clinically defined subclasses of primary LBCLs display site-specific abnormal expression patterns of PcG genes of the HPC-HPH/PRC1 PcG complex. Some of these patterns (such as the expression profile of BMI-1) may be diagnostically relevant. We propose that distinct expression profiles of PcG genes results in abnormal formation of HPC-HPH/PRC1 PcG complexes, and that this contributes to lymphomagenesis and different clinical behavior of clinically defined LBCLs.